How Seriously Should We Take the Promising News on Long COVID?
One of the biggest challenges of the COVID-19 pandemic is the way in which it has forced us to question our hopes. In normal times, hope is a tonic we take in small doses to keep us moving forward through the slog of daily life. The pandemic, however, has made it a much scarcer commodity, spurring us not only to seek it more desperately but to scrutinize it more closely.
Every bit of reassurance seems to come with caveats: Masks can shield us from the coronavirus, but they may need to be doubled in some situations to provide adequate protection. Vaccines work, but they may not be as effective against some viral variants—and they can cause extremely rare but serious side effects. Every few weeks, another potential miracle cure makes headlines (Hydroxychloroquine! Convalescent plasma!), only to prove disappointing on closer inspection. It's hard to know which alleged breakthroughs are worth pinning our hopes on, and which are the products of wishful thinking or hucksterism.
In January 2021, a study published in the journal Gut offered evidence that bacteria in the intestines might influence a whole spectrum of symptoms in long-haul patients.
Lately, two possible sources of hope have emerged concerning so-called "long COVID"—the debilitating syndrome, estimated to affect up to one-third of patients, in which physical, neurological, and cognitive symptoms persist for months. The first encouraging item has gotten plenty of media attention: reports that some long-haulers feel better after being vaccinated. The second item, while less widely covered, has caused a stir among scientists: a study suggesting that rebalancing the gut microbiome—the community of microorganisms in our intestines—could decrease both the severity and duration of the illness.
How optimistic should we allow ourselves to be about either of these developments? Experts warn that it's too soon to tell. Yet research into how vaccines and gut bacteria affect long-haulers—and how both factors might work together—could eventually help solve key pieces of the pandemic puzzle.
Investigating the Role of the Gut Microbiome
The idea that there may be a link between COVID-19 and gut health comes as no surprise to Jessica Lovett. Her case began in June 2020 with gastrointestinal distress—a symptom that was just beginning to be recognized as commonplace in what had initially been considered a respiratory illness. "I had diarrhea three to five times a day for two months," Lovett recalls. "I lost a lot of weight." By July, she was also suffering shortness of breath, chest pain, racing heartbeat, severe fatigue, brain fog, migraines, memory lapses, and more. As with many other COVID long-haulers, these troubles waxed and waned in an endless parade.
Lovett was the marketing manager for a music school in Austin, Texas, and the mother of a two-year-old boy. Just before she got sick, she ran a 5K race for her 40th birthday. Afterward, she had to give up her job, stop driving, and delegate childcare to her husband (who fell ill shortly before she did but recovered in 12 days). Tests showed no visible damage to her lungs, heart, or other organs. But she felt intuitively that taming her GI troubles would be key to getting well. On the advice of fellow patients in a long-COVID Facebook group—and, later, with the guidance of a doctor—she tried avoiding foods thought to trigger histamine reactions or inflammation. That seemed to help some, as did nutritional supplements, antihistamines, and angina medications. Still, she relapsed frequently, and was often bedridden.
In January 2021, a study published in the journal Gut offered evidence that bacteria in the intestines might influence a whole spectrum of symptoms in patients like Lovett. Researchers at the Chinese University of Hong Kong examined blood and stool samples and medical records from 100 hospital patients with lab-confirmed COVID-19 infections, and from 78 people without the disease who were taking part in a microbiome study before the pandemic.
The team, led by professor Siew Chien Ng, found that the makeup of the gut microbiome differed sharply between the two groups. Patients with COVID had higher levels of three bacterial species than those without the infection, but lower levels of several species known to enhance immune system response. Reductions in two of those species—Faecalibacterium prausnitzii and Bifidobacterium bifidum—were associated with more severe symptoms. And the numbers of such helpful bacteria remained low in stool samples collected up to 30 days after infected patients had seemingly cleared the coronavirus from their bodies.
Analysis of blood samples, moreover, showed that these bacterial imbalances correlated with higher levels of inflammatory cytokines (immune system chemicals that are elevated in many patients with severe COVID-19) and markers of tissue damage, such as C-reactive protein.
These findings led the researchers to suggest that rebalancing the microbiome might lessen not only the intensity of COVID symptoms, but also their persistence. "Bolstering of beneficial gut species depleted in COVID-19," they wrote, "could serve as a novel avenue to mitigate severe disease, underscoring the importance of managing patients' gut biota during and after COVID-19."
Soon afterward, Ng revealed that she was working on a solution. Her team, she told Medscape, had developed "a microbiome immunity product that is targeted to what is missing in COVID-19 patients." Early research showed that hospitalized patients who received the treatment developed more antibodies, had fewer symptoms, and were discharged sooner. "So it is quite a bright and promising future," she enthused, "in alleviating some of these detrimental effects of the virus."
The Chicken-and-Egg Problem
Ng's study isn't the only one to suggest a connection between the gut and long COVID. Researchers led by gastroenterologist Saurabh Mehandru at New York's Mount Sinai Hospital recently determined that SARS-CoV-2, the virus that causes COVID-19, can linger in the intestines for months after a patient tests negative. Some studies have also found that gastrointestinal symptoms in the acute phase of the illness correlate with poorer outcomes—though that's far from settled. (In another study, Mehandru's team found lower mortality among patients presenting with GI symptoms.) But the Hong Kong group's paper was the first to posit that resident microbes may play a decisive role in the disease.
That view reflects growing evidence that these bugs can influence a range of ailments, from diabetes to schizophrenia. Over the past decade, the gut microbiome has emerged as a central regulator of the immune system. Some intestinal bacteria emit chemicals that signal immune cells to reduce production of inflammatory proteins, or help those cells effectively target invading pathogens. They also help maintain the integrity of the intestinal lining—preventing the syndrome known as "leaky gut," in which harmful microbes or toxins penetrate to the underlying tissue, potentially wreaking havoc throughout the body and brain.
Nonetheless, many experts have responded to Ng's findings with distinct caution. One problem, they point out, is the chicken-and-egg question: Do reduced levels of beneficial gut bacteria trigger the inflammation seen in COVID-19, or does inflammation triggered by COVID-19 kill off beneficial gut bacteria? "It's an issue of causality versus just association," explains Somsouk Ma, a professor of gastroenterology at the University of California, San Francisco. "I tend to think that the shift in microbes is more likely a consequence of the infection. But, of course, that's just speculation."
A related issue is whether a pill that replenishes "good" bacteria can really combat the effects of COVID-19—whether acute or chronic. Although scientists are studying fecal transplants and other probiotic therapies for many disorders, none has yet been approved by the U.S Food and Drug Administration. "The only situation where bacterial transplantation is known to work is in a form of colitis called Clostridium difficile," notes Mehandru. "I think it's a bit premature to lay too much emphasis on this in the context of COVID."
Placebo-controlled clinical trials will be needed to determine the efficacy of Ng's approach. (Consumer warning: The bacteria she's employing are not found in commercially available probiotics.) Whatever the results, such research—along with studies that track patients' gut microbiomes before, during, and after COVID-19 infection—could help scientists understand why some people have such trouble kicking the disease.
An Unexpected Benefit of Vaccines
The question of what causes long COVID is also central to understanding the effects of vaccines on the condition. In March, as inoculation campaigns took off across the nation, many long-haulers were delighted to see their symptoms disappear within days of getting the shot. "I woke up and it was like, 'Oh what a beautiful morning,'" one patient told The New York Times.
Yet the effects have been far from uniform. Although scientific surveys have not yet been conducted, an April poll by a Facebook group called Survivor Corps found numbers close to experts' estimates: 39 percent said they experienced partial to full recovery post-vaccination; 46 percent saw no difference; and 14 percent felt worse.
How could vaccines—which are designed to prevent COVID-19, not cure it—help some chronic patients get well? In a blog post, Yale immunologist Akiko Iwasaki suggested that the answer depends on what is driving a particular patient's symptoms. Iwasaki identified three possible mechanisms behind long COVID: 1) a persistent viral reservoir; 2) a "viral ghost," composed of fragments of the virus (RNA or proteins) that linger after the infection has been cleared but can still stimulate inflammation; and 3) an autoimmune response triggered by the infection, inducing a patient's immune cells to attack her own tissues.
These mechanisms "are not mutually exclusive," Iwasaki wrote, "and all three might benefit from the vaccines." If a patient has a viral reservoir, vaccine-induced immune cells and antibodies might be able to eliminate it. If the patient has a viral ghost, those vaccine-primed immune responses might knock it out as well. And if the patient is suffering from a COVID-triggered autoimmune syndrome, the vaccine might act as a decoy, shifting the immune system's attention to antigens contained in the shot (and perhaps reprogramming autoimmune cells in the process). The varying role of these underlying factors, and possibly others—such as the gut microbiome—might also help explain why vaccines don't benefit all long-haulers equally. Iwasaki and her team recently launched a clinical study to investigate this theory.
Pato Hebert, a professor of art and public policy at NYU, contracted COVID-19 in March 2020 while on sabbatical in Los Angeles. Hebert, then 50, started out with mild flu-like symptoms, but he was slammed with fatigue, headaches, and confusion a week after testing positive. In April, he landed in urgent care with severe shortness of breath. His brain fog worsened that summer, and a gentle swim brought on a dizzy spell so overwhelming that he feared it was a stroke. (Thankfully, tests showed it wasn't.) In September, he developed severe GI issues, which came and went over the following months. He found some relief through medications, dietary adjustments, acupuncture, herbal remedies, and careful conservation of his physical and mental energy—but a year after his diagnosis, he was still sick.
Hebert received his first dose of the Moderna vaccine on March 1, 2021; it made no difference in his symptoms. After his second dose, on the 29th, he suffered terrible headaches—"like early COVID days," he told me. A week later, his condition had improved slightly compared to pre-vaccination. "With a few exceptions, my fatigue and brain fog have been less challenging," he reported. "I'm cautiously optimistic." But in late April, he suffered another flareup of respiratory and GI issues.
For Jessica Lovett, the vaccine's effects were more dramatic. After her first dose of the Pfizer-BioNTech formula, on February 26, her cognitive symptoms improved enough that she was able to drive again; within a week, she was pushing her son uphill in a stroller, lifting light weights, and running for short distances. After the second dose, she says, "I had incredible energy. It was insane, like I drank three cups of coffee."
Lovett (who now runs a Facebook support group for Austin locals, ATX Covid Long Haulers) stresses that the vaccine hasn't cured her. She winds up back in bed whenever she pushes herself too hard. She still needs to take antihistamines and shun certain foodstuffs; any slip-up brings another relapse. Yet she's able to live more fully than at any time since she fell ill—and she has begun to feel a renewed sense of hope.
Recently, in fact, she and her husband decided to expand their family. "I guess that tells you something," she says with a laugh. "The doctors have given us the okay, and we're going to try."
New tech for prison reform spreads to 11 states
A new non-profit called Recidiviz is using data technology to reduce the size of the U.S. criminal justice system. The bi-coastal company (SF and NYC) is currently working with 11 states to improve their systems and, so far, has helped remove nearly 69,000 people — ones left floundering in jail or on parole when they should have been released.
“The root cause is fragmentation,” says Clementine Jacoby, 31, a software engineer who worked at Google before co-founding Recidiviz in 2019. In the 1970s and 80s, the U.S. built a series of disconnected data systems, and this patchwork is still being used by criminal justice authorities today. It requires parole officers to manually calculate release dates, leading to errors in many cases. “[They] have done everything they need to do to earn their release, but they're still stuck in the system,” Jacoby says.
Recidiviz has built a platform that connects the different databases, with the goal of identifying people who are already qualified for release but remain behind bars or on supervision. “Think of Recidiviz like Google Maps,” says Jacoby, who worked on Maps when she was at the tech giant. Google Maps takes in data from different sources – satellite images, street maps, local business data — and organizes it into one easy view. “Recidiviz does something similar with criminal justice data,” Jacoby explains, “making it easy to identify people eligible to come home or to move to less intensive levels of supervision.”
People like Jacoby’s uncle. His experience with incarceration is what inspired her passion for criminal justice reform in the first place.
The problems are vast
The U.S. has the highest incarceration rate in the world — 2 million people according to the watchdog group, Prison Policy Initiative — at a cost of $182 billion a year. The numbers could be a lot lower if not for an array of problems including inaccurate sentencing calculations, flawed algorithms and parole violations laws.
Sentencing miscalculations
To determine eligibility for release, the current system requires corrections officers to check 21 different requirements spread across five different databases for each of the 90 to 100 people under their supervision. These manual calculations are time prohibitive, says Jacoby, and fall victim to human error.
In addition, Recidiviz found that policies aimed at helping to reduce the prison population don’t always work correctly. A key example is time off for good behavior laws that allow inmates to earn one day off for every 30 days of good behavior. Some states' data systems are built to calculate time off as one day per month of good behavior, rather than per day. Over the course of a decade-long sentence, Jacoby says these miscalculations can lead to a huge discrepancy in the calculated release data and the actual release date.
Algorithms
Commercial algorithm-based software systems for risk assessment continue to be widely used in the criminal justice system, even though a 2018 study published in Science Advances exposed their limitations. After the study went viral, it took three years for the Justice Department to issue a report on their own flawed algorithms used to reduce the federal prison population as part of the 2018 First Step Act. The program, it was determined, overestimated the risk of putting inmates of color into early-release programs.
Despite its name, Recidiviz does not build these types of algorithms for predicting recidivism, or whether someone will commit another crime after being released from prison. Rather, Jacoby says the company’s "descriptive analytics” approach is specifically intended to weed out incarceration inequalities and avoid algorithmic pitfalls.
Parole violation laws
Research shows that 350,000 people a year — about a quarter of the total prison population — are sent back not because they’ve committed another crime, but because they’ve broken a specific rule of their probation. “Things that wouldn't send you or I to prison, but would send someone on parole,” such as crossing county lines or being in the presence of alcohol when they shouldn’t be, are inflating the prison population, says Jacoby.
It’s personal for the co-founder and CEO
“I grew up with an uncle who went into the prison system,” Jacoby says. At 19, he was sentenced to ten years in prison for a non-violent crime. A few months after being released from jail, he was sent back for a non-violent parole violation.
“For my family, the fact that one in four prison admissions are driven not by a crime but by someone who's broken a rule on probation and parole was really profound because that happened to my uncle,” Jacoby says. The experience led her to begin studying criminal justice in high school, then college. She continued her dive into how the criminal justice system works as part of her Passion Project while at Google, a program that allows employees to spend 20 percent of their time on pro-bono work. Two colleagues whose family members had also been stuck in the system joined her.
As part of the project, Jacoby interviewed hundreds of people involved in the criminal justice system. “Those on the right, those on the left, agreed that bad data was slowing down reform,” she says. Their research brought them to North Dakota where they began to understand the root of the problem. The corrections department is making “huge, consequential decisions every day [without] … the data,” Jacoby says. In a new video by Recidiviz not yet released, Jacoby recounts her exchange with the state’s director of corrections who told her, “‘It’s not that we have the data and we just don’t know how to make it public; we don’t have the information you think we have.'"
A mock-up (with fake data) of the types of dashboards and insights that Recidiviz provides to state governments.
Recidiviz
As a software engineer, Jacoby says the comment made no sense to her — until she witnessed it first-hand. “We spent a lot of time driving around in cars with corrections directors and parole officers watching them use these incredibly taxing, frankly terrible, old data systems,” Jacoby says.
As they weeded through thousands of files — some computerized, some on paper — they unearthed the consequences of bad data: Hundreds of people in prison well past their release date and thousands more whose release from parole was delayed because of minor paperwork issues. They found individuals stuck in parole because they hadn’t checked one last item off their eligibility list — like simply failing to provide their parole officer with a paystub. And, even when parolees advocated for themselves, the archaic system made it difficult for their parole officers to confirm their eligibility, so they remained in the system. Jacoby and her team also unpacked specific policies that drive racial disparities — such as fines and fees.
The Solution
It’s more than a trivial technical challenge to bring the incomplete, fragmented data onto a 21st century data platform. It takes months for Recidiviz to sift through a state’s information systems to connect databases “with the goal of tracking a person all the way through their journey and find out what’s working for 18- to 25-year-old men, what’s working for new mothers,” explains Jacoby in the video.
TED Talk: How bad data traps people in the U.S. justice system
TED Fellow Clementine Jacoby's TED Talk went live on Jan. 13. It describes how we can fix bad data in the criminal justice system, "bringing thousands of people home, reducing costs and improving public safety along the way."
Clementine Jacoby • TED2022
Ojmarrh Mitchell, an associate professor in the School of Criminology and Criminal Justice at Arizona State University, who is not involved with the company, says what Recidiviz is doing is “remarkable.” His perspective goes beyond academic analysis. In his pre-academic years, Mitchell was a probation officer, working within the framework of the “well known, but invisible” information sharing issues that plague criminal justice departments. The flexibility of Recidiviz’s approach is what makes it especially innovative, he says. “They identify the specific gaps in each jurisdiction and tailor a solution for that jurisdiction.”
On the downside, the process used by Recidiviz is “a bit opaque,” Mitchell says, with few details available on how Recidiviz designs its tools and tracks outcomes. By sharing more information about how its actions lead to progress in a given jurisdiction, Recidiviz could help reformers in other places figure out which programs have the best potential to work well.
The eleven states in which Recidiviz is working include California, Colorado, Maine, Michigan, Missouri, Pennsylvania and Tennessee. And a pilot program launched last year in Idaho, if scaled nationally, with could reduce the number of people in the criminal justice system by a quarter of a million people, Jacoby says. As part of the pilot, rather than relying on manual calculations, Recidiviz is equipping leaders and the probation officers with actionable information with a few clicks of an app that Recidiviz built.
Mitchell is disappointed that there’s even the need for Recidiviz. “This is a problem that government agencies have a responsibility to address,” he says. “But they haven’t.” For one company to come along and fill such a large gap is “remarkable.”
How Leqembi became the biggest news in Alzheimer’s disease in 40 years, and what comes next
A few months ago, Betsy Groves traveled less than a mile from her home in Cambridge, Mass. to give a talk to a bunch of scientists. The scientists, who worked for the pharmaceutical companies Biogen and Eisai, wanted to know how she lived her life, how she thought about her future, and what it was like when a doctor’s appointment in 2021 gave her the worst possible news. Groves, 73, has Alzheimer’s disease. She caught it early, through a lumbar puncture that showed evidence of amyloid, an Alzheimer’s hallmark, in her cerebrospinal fluid. As a way of dealing with her diagnosis, she joined the Alzheimer’s Association’s National Early-Stage Advisory Board, which helped her shift into seeing her diagnosis as something she could use to help others.
After her talk, Groves stayed for lunch with the scientists, who were eager to put a face to their work. Biogen and Eisai were about to release the first drug to successfully combat Alzheimer’s in 40 years of experimental disaster. Their drug, which is known by the scientific name lecanemab and the marketing name Leqembi, was granted accelerated approval by the U.S. Food and Drug Administration last Friday, Jan. 6, after a study in 1,800 people showed that it reduced cognitive decline by 27 percent over 18 months.
It is no exaggeration to say that this result is a huge deal. The field of Alzheimer’s drug development has been absolutely littered with failures. Almost everything researchers have tried has tanked in clinical trials. “Most of the things that we've done have proven not to be effective, and it's not because we haven’t been taking a ton of shots at goal,” says Anton Porsteinsson, director of the University of Rochester Alzheimer's Disease Care, Research, and Education Program, who worked on the lecanemab trial. “I think it's fair to say you don't survive in this field unless you're an eternal optimist.”
As far back as 1984, a cure looked like it was within reach: Scientists discovered that the sticky plaques that develop in the brains of those who have Alzheimer’s are made up of a protein fragment called beta-amyloid. Buildup of beta-amyloid seemed to be sufficient to disrupt communication between, and eventually kill, memory cells. If that was true, then the cure should be straightforward: Stop the buildup of beta-amyloid; stop the Alzheimer’s disease.
It wasn’t so simple. Over the next 38 years, hundreds of drugs designed either to interfere with the production of abnormal amyloid or to clear it from the brain flamed out in trials. It got so bad that neuroscience drug divisions at major pharmaceutical companies (AstraZeneca, Pfizer, Bristol-Myers, GSK, Amgen) closed one by one, leaving the field to smaller, scrappier companies, like Cambridge-based Biogen and Tokyo-based Eisai. Some scientists began to dismiss the amyloid hypothesis altogether: If this protein fragment was so important to the disease, why didn’t ridding the brain of it do anything for patients? There was another abnormal protein that showed up in the brains of Alzheimer’s patients, called tau. Some researchers defected to the tau camp, or came to believe the proteins caused damage in combination.
The situation came to a head in 2021, when the FDA granted provisional approval to a drug called aducanumab, marketed as Aduhelm, against the advice of its own advisory council. The approval was based on proof that Aduhelm reduced beta-amyloid in the brain, even though one research trial showed it had no effect on people’s symptoms or daily life. Aduhelm could also cause serious side effects, like brain swelling and amyloid related imaging abnormalities (known as ARIA, these are basically micro-bleeds that appear on MRI scans). Without a clear benefit to memory loss that would make these risks worth it, Medicare refused to pay for Aduhelm among the general population. Two congressional committees launched an investigation into the drug’s approval, citing corporate greed, lapses in protocol, and an unjustifiably high price. (Aduhelm was also produced by the pharmaceutical company Biogen.)
To be clear, Leqembi is not the cure Alzheimer’s researchers hope for. While the drug is the first to show clear signs of a clinical benefit, the scientific establishment is split on how much of a difference Leqembi will make in the real world.
So far, Leqembi is like Aduhelm in that it has been given accelerated approval only for its ability to remove amyloid from the brain. Both are monoclonal antibodies that direct the immune system to attack and clear dysfunctional beta-amyloid. The difference is that, while that’s all Aduhelm was ever shown to do, Leqembi’s makers have already asked the FDA to give it full approval – a decision that would increase the likelihood that Medicare will cover it – based on data that show it also improves Alzheimer’s sufferer’s lives. Leqembi targets a different type of amyloid, a soluble version called “protofibrils,” and that appears to change the effect. “It can give individuals and their families three, six months longer to be participating in daily life and living independently,” says Claire Sexton, PhD, senior director of scientific programs & outreach for the Alzheimer's Association. “These types of changes matter for individuals and for their families.”
To be clear, Leqembi is not the cure Alzheimer’s researchers hope for. It does not halt or reverse the disease, and people do not get better. While the drug is the first to show clear signs of a clinical benefit, the scientific establishment is split on how much of a difference Leqembi will make in the real world. It has “a rather small effect,” wrote NIH Alzheimer’s researcher Madhav Thambisetty, MD, PhD, in an email to Leaps.org. “It is unclear how meaningful this difference will be to patients, and it is unlikely that this level of difference will be obvious to a patient (or their caregivers).” Another issue is cost: Leqembi will become available to patients later this month, but Eisai is setting the price at $26,500 per year, meaning that very few patients will be able to afford it unless Medicare chooses to reimburse them for it.
The same side effects that plagued Aduhelm are common in Leqembi treatment as well. In many patients, amyloid doesn’t just accumulate around neurons, it also forms deposits in the walls of blood vessels. Blood vessels that are shot through with amyloid are more brittle. If you infuse a drug that targets amyloid, brittle blood vessels in the brain can develop leakage that results in swelling or bleeds. Most of these come with no symptoms, and are only seen during testing, which is why they are called “imaging abnormalities.” But in situations where patients have multiple diseases or are prescribed incompatible drugs, they can be serious enough to cause death. The three deaths reported from Leqembi treatment (so far) are enough to make Thambisetty wonder “how well the drug may be tolerated in real world clinical practice where patients are likely to be sicker and have multiple other medical conditions in contrast to carefully selected patients in clinical trials.”
Porsteinsson believes that earlier detection of Alzheimer’s disease will be the next great advance in treatment, a more important step forward than Leqembi’s approval.
Still, there are reasons to be excited. A successful Alzheimer’s drug can pave the way for combination studies, in which patients try a known effective drug alongside newer, more experimental ones; or preventative studies, which take place years before symptoms occur. It also represents enormous strides in researchers’ understanding of the disease. For example, drug dosages have increased massively—in some cases quadrupling—from the early days of Alzheimer’s research. And patient selection for studies has changed drastically as well. Doctors now know that you’ve got to catch the disease early, through PET-scans or CSF tests for amyloid, if you want any chance of changing its course.
Porsteinsson believes that earlier detection of Alzheimer’s disease will be the next great advance in treatment, a more important step forward than Leqembi’s approval. His lab already uses blood tests for different types of amyloid, for different types of tau, and for measures of neuroinflammation, neural damage, and synaptic health, but commercially available versions from companies like C2N, Quest, and Fuji Rebio are likely to hit the market in the next couple of years. “[They are] going to transform the diagnosis of Alzheimer's disease,” Porsteinsson says. “If someone is experiencing memory problems, their physicians will be able to order a blood test that will tell us if this is the result of changes in your brain due to Alzheimer's disease. It will ultimately make it much easier to identify people at a very early stage of the disease, where they are most likely to benefit from treatment.”
Learn more about new blood tests to detect Alzheimer's
Early detection can help patients for more philosophical reasons as well. Betsy Groves credits finding her Alzheimer’s early with giving her the space to understand and process the changes that were happening to her before they got so bad that she couldn’t. She has been able to update her legal documents and, through her role on the Advisory Group, help the Alzheimer’s Association with developing its programs and support services for people in the early stages of the disease. She still drives, and because she and her husband love to travel, they are hoping to get out of grey, rainy Cambridge and off to Texas or Arizona this spring.
Because her Alzheimer’s disease involves amyloid deposits (a “substantial portion” do not, says Claire Sexton, which is an additional complication for research), and has not yet reached an advanced stage, Groves may be a good candidate to try Leqembi. She says she’d welcome the opportunity to take it. If she can get access, Groves hopes the drug will give her more days to be fully functioning with her husband, daughters, and three grandchildren. Mostly, she avoids thinking about what the latter stages of Alzheimer’s might be like, but she knows the time will come when it will be her reality. “So whatever lecanemab can do to extend my more productive ways of engaging with relationships in the world,” she says. “I'll take that in a minute.”